Ali Muhammad, Li Yabing, O'Neal Wesley T, Soliman Elsayed Z
Department of Internal Medicine, Section on Hospital Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Epidemiological Cardiology Research Center (EPICARE), Department of Epidemiology and Prevention, Wake Forest School of Medicine, Winston Salem, North Carolina.
Am J Cardiol. 2017 Oct 1;120(7):1114-1117. doi: 10.1016/j.amjcard.2017.06.050. Epub 2017 Jul 14.
Tobacco exposure including second-hand smoke is the leading preventable cause of premature death in the United States. Serum cotinine, a highly sensitive and specific biomarker for tobacco exposure, is a more accurate measure of tobacco exposure than self-reported smoking status. Although the harmful effect of tobacco exposure on cardiovascular disease (CVD) risk factors (e.g., atherosclerosis) or hard CVD outcomes (e.g., myocardial infarction) is well established, its effect on intermediate outcomes such as subclinical myocardial injury (SMI), especially in nonsmokers, is not clear. Therefore, we examined the risk of SMI, defined as a Cardiac Infarction/Injury Score of ≥10 points on the 12-lead electrocardiogram with abnormal serum cotinine levels (>15 ng/ml) in 6,264 smokers and nonsmokers who were free from CVD enrolled in the Third National Health and Nutrition Examination Survey. SMI was more common in those with abnormal compared with normal serum cotinine levels (25.9% vs 19.6%, respectively; p <0.01). In a multivariable logistic regression model adjusted for age, gender, race, obesity, diabetes, hypertension, and dyslipidemia, abnormal (vs normal) serum cotinine was associated with a 61% increased risk of SMI (odds ratio 1.61, 95% confidence interval 1.40 to 1.85, p <0.01). This association was stronger in smokers, in women, and in nondiabetic and nonobese participants. In conclusion, elevated serum cotinine levels are associated with an increased risk of SMI in participants free from CVD, and this association is stronger in certain groups of participants. These findings underscore the harmful effect of both active and passive tobacco exposures on the cardiovascular system, and highlight the need for a personalized risk assessment that takes into account groups at high risk.
在美国，包括二手烟在内的烟草暴露是可预防的过早死亡的主要原因。血清可替宁是一种对烟草暴露高度敏感且特异的生物标志物，相较于自我报告的吸烟状况，它是衡量烟草暴露更准确的指标。尽管烟草暴露对心血管疾病（CVD）危险因素（如动脉粥样硬化）或严重CVD结局（如心肌梗死）的有害影响已得到充分证实，但其对亚临床心肌损伤（SMI）等中间结局的影响，尤其是在非吸烟者中，尚不清楚。因此，我们在参加第三次全国健康与营养检查调查且无CVD的6264名吸烟者和非吸烟者中，研究了血清可替宁水平异常（>15 ng/ml）且12导联心电图上心肌梗死/损伤评分≥10分所定义的SMI风险。血清可替宁水平异常者的SMI比正常者更常见（分别为25.9%和19.6%；p<0.01）。在调整了年龄、性别、种族、肥胖、糖尿病、高血压和血脂异常的多变量逻辑回归模型中，血清可替宁异常（与正常相比）与SMI风险增加61%相关（比值比1.61，95%置信区间1.40至1.85，p<0.01）。这种关联在吸烟者、女性以及非糖尿病和非肥胖参与者中更强。总之，血清可替宁水平升高与无CVD参与者的SMI风险增加相关，且这种关联在某些参与者群体中更强。这些发现强调了主动和被动烟草暴露对心血管系统的有害影响，并突出了进行个性化风险评估以考虑高危群体的必要性。
